Mechanisms of resistance to and transmission of galbut virus in Drosophila melanogaster

Abstract

The advent of sequencing has opened doors into worlds unseen before. We now know that organisms can be infected by many microorganisms at once, often with no apparent signs or symptoms. Many viruses lie in wait for the lifetime of their hosts before being transmitted to offspring to continue the cycle. To build on a body of work dedicated to uncovering the ways that persistent viruses impact their hosts, I have investigated the host-virus relationship between the model organism Drosophila melanogaster and its most successful natural virus, galbut virus. In Chapter 1, I present the case for studying persistent viruses and vertical transmission and provide background on partitiviruses and the D. melanogaster model system. In Chapter 2, I identify a mechanism of cross contamination of RNA from stored frozen samples. This cross contamination was sufficient to skew qPCR identification of both viral and host RNAs. This work changed collection and storage methods that we employed in the lab to limit false qPCR results in studies of prevalence. In Chapter 3, I describe my work identifying genes associated with resistance to galbut virus in multiple independent populations. This work revealed categories of genes that may be drivers of resistance to persistent viruses, opening the door for functional studies that can confirm their roles in resistance and underlying mechanisms. In Chapter 4, I describe a large study of multigenerational vertical transmission efficiency as a function of sex and genetic background that relates to persistence of galbut virus in nature. I was able to identify a significant sex bias in the transmission of galbut virus through several generations. In summary, my dissertation contributes to a better understanding of the relationship between hosts and their persistent viruses, and the basis for their success in nature.